Resistance to pathogens is thought to involve a specific recognition between a resistant plant and the pathogen, which triggers a set of responses that act to confine the pathogen. The specificity of this process is considered to involve a recognition between the products of a plant resistance (R) gene and a cognate pathogen avirulence gene (Dangl, 1995; Staskawicz et al., 1995). The characterization of resistance genes is of major importance for elucidating the initiation of the cascade of events that leads to specific resistance responses, as well as for more efficient introduction of resistance to pathogens into important crops.
Several resistance genes have been cloned recently by positional cloning or by transposon tagging. These genes include: the HM1 gene of maize (Johal and Briggs, 1992), the Pto gene of tomato (Martin et al., 1993), the Cf-9 gene of tomato (Jones et al., 1994), the RPS2 (Bent et al., 1994; Mindrinos et al., 1994) and the RPM1 (Grant, 1995) genes from Arabidopsis, the N gene from tobacco (Whitham et al., 1994), and the L6 gene from flax (Ellis et al., 1995; Lawrence et al, 1995). These resistance genes show diverse biological characteristics. The HM1 gene is the only example to date where the gene product acts directly to inactivate a component of the pathogen attack, or a compatibility factor (Briggs and Johal, 1994). The other genes belong to a different genetic category, that of incompatibility (or gene for gene) interaction, based on the recognition by the resistance gene product of in avirulence (or incompatibility) component of the pathogen, which does not necessarily participate in the compatibility or in the infection processes (Briggs and Johal, 1994). These genes are all involved in resistance processes characterized by hypersensitive response (HR). In spite of their origin from different plant species, and their divergent specificity to viral, fungal or bacterial pathogens, a group of these R genes share several structural features. A nucleotide-binding domain (P-loop) and five additional amino-acid stretches of unknown function are conserved in their N-terminal region. A region of leucine-rich repeats (LRR) is present in their C terminus, though the consensus sequence and the length of the repeats are different among them. LRR were shown to be involved in protein-protein interactions in other proteins (Kobe and Deisenhofer, 1994; Kobe and Deisenhofer, 1995), and may have similar role in resistance genes. The N gene, the L6 gene and the Cf-9 gene were shown to belong to large gene families, partially clustered with the resistance gene. The detailed genomic distribution of these multigene families is yet unknown.
The soil-born fungus Fusarium oxysporum is the causative agent of severe will diseases in a large variety of plant species world-wide. It is an imperfect fungus for which no sexual cycle is known. The tomato-specific pathogen Fusarium oxysporum f. sp. lycopersici (F.o.l) causes the disease Fusarium wilt. The fungus penetrates the vascular system of roots from both resistant and susceptible varieties, mainly through wounds. During a compatible interaction, which leads to disease, the fungus proceeds through the vascular system which eventually collapses. This leads to wilt and often to death of the plant. During an incompatible interaction, resulting in resistance, the fungus is confined to the lower part of the roots, and further symptoms do not develop. Several mechanisms, not including HR, were suggested to be involved in this resistance. They include: the production of inhibitory secondary metabolites, and structural barriers such as vascular gelation, callose deposition, and abnormal membrane outgrowths of vascular parenchyma cells, termed tyloses. Most of these processes, thought to be involved in resistance to vascular diseases, are detectabe also in compatible interactions, though to a lesser extent. Therefore the exact sequence of events that leads to resistance is still unknown.
Three races of F.o.l. and their cognate R genes have been identified in tomato. The classification of different F.o.l. isolates into races does not correlate with their general genetic resemblance, as established by restriction fragment length polymorphism (RFLP) analysis and distribution into vegetative compatibility groups (VCG; Elias et al., 1993). The I locus, introgressed from L. pimpinellifolium, confers resistance to F.o.l race 1, and is located on the short arm of chromosome 11, between the RFLP markers TG523 and CP58 (Eshed and Ori, unpublished). The I3 locus from chromosome 7 of L. pennellii confers resistance to races 1, 2 and 3 of F.o.l. (Bournival et al., 1990). This locus appears to be composed of three separate but linked genes (Scott and Jones, 1991). The I2 locus, introgressed from L. pimpinellifolium, confers resistance to race 2 of the pathogen. We previously mapped I2 to the long arm of chromosome 11, between the RFLP markers TG105 and TG36, very close to TG105 (Segal et al., 1992; Ori et al., 1994). In previous studies we utilized recombinant inbred (RI) lines for mapping I2 (Ori et al., 1994). However this population turned to be problematic for mapping of this region because of a very high recombination rate, including double recombinations, especially in the region of I2.